Acute Respiratory Distress Syndrome

ARDS

Lung complication resulting in dangerously low blood

oxygen

ARDS is often a result of other health complications

Clinical Manifestations

Related to systemic

inflammatory disease

Bilateral pulmonary

infiltration

Increased pulmonary

capillary permeability

Decreased PaO2/FiO2

ratio

Severity Stages

New classification system

Better predictor of mortality

Three classifications:

Mild PaO2/FiO2 <300 mmHg

Acute lung injury

Moderate <200 mmHg

Severe <100 mmHg

75% of cases are classified moderate or severe

Incidence

9% incidence of ARDS and ALL in the ICU

United States: 64:100,000

Europe: 4.9-13.5:100,000

American Lung Association: 1.5-75 cases/100,000

individuals

25-40% of cases end in death

Increasing Incidence of ARDS cases

Life Expectancy

Dependent of cause of ARDS

Patients with fewer chronic diseases have increased survival

Sepsis induced ARDS has increased risk of mortality

Pulmonary fibrosis is found to be a major factor

1988: 50-70% mortality

2008: 25-40% mortality

Death typically results from MODS from a lack of oxygen

rather than lung failure

Decreasing mortality risk for ARDS patients

Etiology

Direct injury:

Trauma

Aspiration

Inhaling Chemicals

Obstructed airways

Indirect injury

Blood transfusion

Sepsis

Pneumonia

Signs and Symptoms

Depending on the initial trauma specific S/S can occur

Ex. Pneumonia cough

Difficulty breathing

Two-pillow orthopnea: support from pillows to in order to easy

breathing that occurs from the recumbent position

Rapid breathing

Shortness of Breath

Low blood oxygen level

S/S continued Trachea shift: trachea shifts

from its normal position because of fluid accumulation in the pleural space

Jugular distention: jugular veins bulge because of increased central venous pressure

Bruit: “noise” unusual sound blood makes when passing an obstruction Medical professionals will

look for bruit sounds to R/O other diseases

Pathophysiology Early phase: exudative (oozing)

Occur as a result of direct or indirect lung insults Acute inflammatory stage with proinflammatory cytokines, neutrophils,

and overall impaired endothelial cell barrier function

Barrier between the capillaries and the alveoli allow water movement into the alveoli

Most patients will survive this stage

Later phase: fibroproliferative

Alveolar damage

Collagen deposition appears in 3 days; Fibrosis manifests within 3 weeks

Pulmonary fibrosis resulting in 55% of ARDS deaths

Risk Factors

Old age

Shock

Liver failure

Patients with diabetes have half the risk for developing ARDS

compared to patients without diabetes

Quality of Life Poor muscle function

Pulmonary function returns to normal or near normal at approx. 6 months

Decrease carbon monoxide diffusion capacity

Memory loss: due to brain damage from lack of oxygen

Fatigue

Weakness

Alopecia

Pain from chest tubes

Entrapment Neuropathy

Heterotopic Ossification

Medical Therapy

Diagnosis

Challenging because ARDS has nonspecific characteristics

48% of patients with autopsy-prove ARDS had ARDS diagnosis

in their charts

Rule out other diseases

Left heart failure

Check left heart function

Acute lung injury

Less severe impairment of oxygen; PaO2/FiO2 <300 mmHg

Goals of Treatment

Support breathing

Treat underlying cause

Medications to treat infections, reduce inflammation, and

remove fluid from the lungs.

Health Impact

25-40% of cases are fatal

By 7-10 days a patient has

died or have been weaned

off treatment

Collapsed Lung

Pneumothorax

Air escapes from the lung

and fills the space outside

the lung.

Smokers, COPD, asthma,

cystic fibrosis, tuberculosis

Collapsed Lung

Increased Risk

Smokers

COPD

Asthma

Cystic fibrosis

Tuberculosis

Symptoms

Sharp chest pain

Shortness of breath

Bluish color

Easy fatigue

Rapid heart rate

Treatment

Small pneumothorax

Can go away on its own

Large Pneumothorax

Chest tube

Surgery

Pleurodesis

Surgery

Treat collapsed lung

Stop fluid buildup

Pulmonary Fibrosis

Scarring throughout the lungs

Prevention of ARDS

No drug has proved beneficial in prevention

Corticosteroids

High-dose corticosteroids

Patients with ARDS persisting for at least 7 days had no benefit

in 60 day mortality

Patients treated 14 days after onset had worsened mortality

with corticosteroid therapy

Methylprednisone

No survival advantage shown

short-term clinical benefits included improved oxygenation and

increased ventilator-free and shock-free days

more likely to experience neuromuscular weakness, but the rate

of infectious complications was not increased.

Corticosteroids Summary

may be considered a form of rescue therapy

may improve oxygenation and hemodynamics

does not change mortality

corticosteroids increase mortality in patients who have had

ARDS for >14 d

Statins

Somovstatin

Preadmission use of statins was associated with a reduction in

30-day and 1-year mortality of a cohort of 12,483 critically ill

patients.

Patients under statin treatment developing MODS have a better

outcome than age- and sex-matched MODS patients without

statin therapy.

TNF and IL-1

Small sepsis trials suggest a potential role for antibody to

tumor necrosis factor (TNF) and recombinant interleukin

(IL)-1 receptor antagonist.

Prostacycline

Prostacycline

Inhaled prostacycline also has not been shown to improve

survival.

Nitric Oxide

Inhaled nitric oxide did not change mortality rates in adults

with ARDS.

Improves transient oxygenation

Side Effects

Short-term

Long-term

Muscle wasting and weakness

Mechanical Ventilation

Ventilation

A ventilator doesn’t treat a disease or condition

GOAL: provide breathing support, relieve respiratory

muscles of their work

Ventilation Benefits

Get oxygen into the lungs

Help people breathe easier – relieve respiratory muscles

Provide breathing support

Mask Ventilation

Intubation

Tube is placed in patients mouth and down into the windpipe

High vs. Low Tidal Volume

High Tidal Volume Low Tidal Volume

Over-distend alveoli

Worsen lung injury

Inflammation

Decreased ventilator-

associated lung injury

Increases survival rate

Recommended to use Low Tidal Volume for ARDS

Positive End-Expiratory Pressure

(PEEP)

Airway pressure is maintained above atmospheric pressure at

the end of exhalation

increase volume of gas remaining in the lungs at the end of

expiration

Decrease shunting of blood through lungs and improve gas

exchange

Purpose: Prevent lungs from collapsing

Prone Positioning

Supine: weight of heart and abdominal

organs on lungs contribute to low

compliancy

Prone: improves oxygenation but does

not improve survival

Higher incidence of complications (i.e.

pressure sores and obstruction of the

endotracheal tube)

Weaning from Mechanical Ventilation

Those who wean successfully have less morbidity and

mortality

Spontaneous breathing trials (SBTs)

Progressive decreases in the level of pressure support during

pressure support ventilation

Extracorporeal Membrane Oxygenation

(ECMO)

Blood circulates

outside of body with

help of a machine

Provides oxygenation

and takes out CO2

For severely/non-functional lungs

The Cochrane Library http://onlinelibrary.wiley.com.erl.lib.byu.edu/doi/10.1002/14651858.CD00

3844.pub4/full

Primary outcome

Mortality

Secondary Outcomes Development of multiple organ failure

Duration of mechanical ventilation

Stay in ICU

Long term health related quality of life

Long-term cognitive complications

Hemolung RAS

CO2 removal and less invasive

Similar to dialysis

Uses less blood flow

Smaller catheter

One component system

Active mixing

Battery operated (patient

can move around)

Hemolung RAS

2012

Successful pilot studies

Arterial pCO2 levels reduced by 28% within 24 hours

lessened dyspnea

improved clinical status

effective and stable CO2 removal on the order of 50% of

metabolic production

No unexpected adverse events

All patients were able to avoid intubation

Approved in Canada and Europe

Undergoing large clinical trials

Medical Nutrition Therapy

Medical Nutrition Therapy

MNT GOALS

Hemodynamically stable through fluid administration

Meet nutritional requirements

Facilitate weaning from mechanical ventilation and oxygen

support

Maintain lean body mass

Improve resistance to infection

Restore respiratory muscle and strength

Medical Nutrition Therapy

Fluid administration: Conservative

administration of fluids after resuscitation

Energy Needs: • Calculate with indirect calorimetry (IC)

• Obese individuals : 11-14 kcal/kg or

60%-70% of target value

• Why: High caloric intake increases

levels of CO2.

Medical Nutrition Therapy

Carbohydrate:

Been shown that concentrations of Carbohydrates not as

important as calories provided

Protein:

1.5-2.0 g/kg

For Obese: 2.0-2.5 g/kg

Fat:

Give enough to provide the right amount of calories

Medical Nutrition Therapy

What to monitor and watch closely

CO2

Phosphate

Vitamin A

Vitamin C

Vitamin E

Meet requirements for Essential Fatty Acids

Medical Nutrition Therapy

Enteral Nutrition

Helps maintain GALT

Less likely to overfeed

Reduces ICU and hospital mortality

Parental Nutrition

More likely to overfeed

Used for patients with: Shock, Nonfunctional Gut, and

Peritonitis

Medical Nutrition Therapy Supplementing with arginine, glutamine, omega-3 fatty acids,

and antioxidants?

Improved Oxygenation, Reduced

number of neutrophils, decreased

length of stay, decreased requirement

for mechanical ventilation

No effect on Mortality

Pulmonary Rehabilitation Programs Small portions

Give favorite foods

Medical Nutrition Therapy

Supplementation of Omega 3 over required amounts not

effective.

Do not use RQ for substrate mix

Consider BMI

Case Study: DH

Anthropometrics

Age: 65

Male

Married – lives with wife (62)

4 children not living in the area

Retired manager of local grocery

chain

Height: 5’ 4”

Weight: 122 lbs

BMI: 20.9

UBW: 135 lbs

IBW: 130 lbs

8 lbs under

Case Study: DH

Biochemical Clinical

Hemoglobin – 13.2 (14-17)

Hematocrit – 39 (40-54)

ABG pH – 7.2 (7.35-7.45)

ABG pCO2 – 65 (35-45)

ABG CO2 content – 35 (25-30)

ABG pO2 – 56 (>80)

ABG HCO3- – 38 (24-28)

Extremities: cyanosis, 1+ pitting

edema

R femoral bruit present

Pale skin

Harsh inspiratory breath sounds

noted over right chest – absent

sounds on left

Use accessory muscles at rest

Case Study – DH

Dietary History

General appetite: decreased over

past several weeks

Usual diet:

B: Egg, hot cereal, bread or

muffin, hot tea (with milk and

sugar)

L: soup, sandwich, hot tea (with

milk and sugar)

D: small amount of meat, rice,

2-3 kinds of vegetables, hot tea

(with milk and sugar)

Diagnosed with emphysema more

than 10 years ago

Tobacco use: 2 PPD for 50 years

Alcohol use: 1-2 drinks 1-2

x/week

PES Statement

Inadequate caloric intake related to increased needs from

history of COPD and Acute Respiratory Distress Syndrome as

evidenced by decrease appetite and weight loss.

Oxepa®

Abbott Nutrition product for

modulating Inflammation in Sepsis,

ALI, and ARDS

Benefits:

Improves oxygenation

Decrease time on ventilator

Decreases length of stay in ICU

For sole-source nutrition

Sample Diet Oxepa – 25 kcal/kg for 24 hrs

55kg (122lbs) – 1375 kcals

Protein needs: minimum 82.5 g (1.5-2.0g/kg)

Amount Calories

(kcal)

% in total

Calories

CHO 97 g 388 27

Protein 57.3 g 250.8 18

Fat 86 g 774 55

Fluid 917 ml 0 0

Total

Calories/24

hours

1412